Plasma dopa has been thought to originate from sympathetic nerve endings and to represent the rate of catecholamine synthesis because plasma dihydroxyphenylalanine (dopa) levels in various experiments followed the changes in norepinephrine (NE) synthesis. However, recent studies of the effect of sympathectomy on the dopa content of skeletal muscle, raised the possibility of skeletal muscle as an additional source of circulating dopa. In this study, we examined the neuronal and skeletal muscle contributions to dopa in arterial plasma. Electrical stimulation of the spinal cord of pithed rats has been applied to initiate discharges both of sympathetic neurones resulting in NE release from sympathetic nerve endings and of spinal motoneurones evoking diffuse contraction of skeletal muscle. This stimulation caused marked elevations in arterial plasma NE, dihydroxyphenylglycol (DHPG), and dopa concentrations. Pretreatment with curare, a skeletal muscle relaxant, did not affect NE and DHPG responses but decreased dopa responses by about 50%. Chlorisondamine, a ganglionic blocker, inhibited all NE, DHPG responses, and dopa responses also by 90%. Adrenal-demedullation did not affect electrical stimulation induced dopa responses in pithed rats. In conclusion, dopa is released into the blood stream during sympathetic stimulation and this response can be inhibited by ganglionic blockade. In addition, these results show, that dopa can be released from a non-neural pool, during skeletal muscle contraction.